Artículos de revistas: "Kidney Pathophysiology"

1

Hewitt, Stephen M. y Robert A. Star. "Enlightening kidney pathophysiology". Nature Materials 18, n.º 10 (19 de septiembre de 2019): 1034–35. http://dx.doi.org/10.1038/s41563-019-0490-5.

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2

McCullough, Peter A. "Cardiorenal Syndromes: Pathophysiology to Prevention". International Journal of Nephrology 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/762590.

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There is a strong association between both acute and chronic dysfunction of the heart and kidneys with respect to morbidity and mortality. The complex interrelationships of longitudinal changes in both organ systems have been difficult to describe and fully understand due to a lack of categorization of the common clinical scenarios where these phenomena are encountered. Thus, cardiorenal syndromes (CRSs) have been subdivided into five syndromes which represent clinical vignettes in which both the heart and the kidney are involved in bidirectional injury and dysfunction via a final common pathway of cell-to-cell death and accelerated apoptosis mediated by oxidative stress. Types 1 and 2 involve acute and chronic cardiovascular disease (CVD) scenarios leading to acute kidney injury (AKI) or accelerated chronic kidney disease (CKD). Types 3 and 4 describe AKI and CKD, respectively, leading primarily to heart failure, although it is possible that acute coronary syndromes, stroke, and arrhythmias could be CVD outcomes in these forms of CRS. Finally, CRSs type 5 describe a systemic insult to both heart and the kidneys, such as sepsis, where both organs are injured simultaneously in persons with previously normal heart and kidney function at baseline. Both blood and urine biomarkers, including the assessment of catalytic iron, a critical element to the generation of oxygen-free radicals and oxidative stress, are reviewed in this paper.

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3

Noda, Yumi, Eisei Sohara, Eriko Ohta y Sei Sasaki. "Aquaporins in kidney pathophysiology". Nature Reviews Nephrology 6, n.º 3 (26 de enero de 2010): 168–78. http://dx.doi.org/10.1038/nrneph.2009.231.

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4

Su, Wen, Rong Cao, Xiao-yan Zhang y Youfei Guan. "Aquaporins in the kidney: physiology and pathophysiology". American Journal of Physiology-Renal Physiology 318, n.º 1 (1 de enero de 2020): F193—F203. http://dx.doi.org/10.1152/ajprenal.00304.2019.

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The kidney is the central organ involved in maintaining water and sodium balance. In human kidneys, nine aquaporins (AQPs), including AQP1–8 and AQP11, have been found and are differentially expressed along the renal tubules and collecting ducts with distinct and critical roles in the regulation of body water homeostasis and urine concentration. Dysfunction and dysregulation of these AQPs result in various water balance disorders. This review summarizes current understanding of physiological and pathophysiological roles of AQPs in the kidney, with a focus on recent progress on AQP2 regulation by the nuclear receptor transcriptional factors. This review also provides an overview of AQPs as clinical biomarkers and therapeutic targets for renal diseases.

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5

Che, Ruochen, Yanggang Yuan, Songming Huang y Aihua Zhang. "Mitochondrial dysfunction in the pathophysiology of renal diseases". American Journal of Physiology-Renal Physiology 306, n.º 4 (15 de febrero de 2014): F367—F378. http://dx.doi.org/10.1152/ajprenal.00571.2013.

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Mitochondrial dysfunction has gained recognition as a contributing factor in many diseases. The kidney is a kind of organ with high energy demand, rich in mitochondria. As such, mitochondrial dysfunction in the kidney plays a critical role in the pathogenesis of kidney diseases. Despite the recognized importance mitochondria play in the pathogenesis of the diseases, there is limited understanding of various aspects of mitochondrial biology. This review examines the physiology and pathophysiology of mitochondria. It begins by discussing mitochondrial structure, mitochondrial DNA, mitochondrial reactive oxygen species production, mitochondrial dynamics, and mitophagy, before turning to inherited mitochondrial cytopathies in kidneys (inherited or sporadic mitochondrial DNA or nuclear DNA mutations in genes that affect mitochondrial function). Glomerular diseases, tubular defects, and other renal diseases are then discussed. Next, acquired mitochondrial dysfunction in kidney diseases is discussed, emphasizing the role of mitochondrial dysfunction in the pathogenesis of chronic kidney disease and acute kidney injury, as their prevalence is increasing. Finally, it summarizes the possible beneficial effects of mitochondrial-targeted therapeutic agents for treatment of mitochondrial dysfunction-mediated kidney injury-genetic therapies, antioxidants, thiazolidinediones, sirtuins, and resveratrol-as mitochondrial-based drugs may offer potential treatments for renal diseases.

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6

Gilbert, Bruce R. y E. Darracott Vaughan. "Pathophysiology of the Aging Kidney". Clinics in Geriatric Medicine 6, n.º 1 (febrero de 1990): 13–30. http://dx.doi.org/10.1016/s0749-0690(18)30631-1.

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7

Nakano, Daisuke y Akira Nishiyama. "Multiphoton imaging of kidney pathophysiology". Journal of Pharmacological Sciences 132, n.º 1 (septiembre de 2016): 1–5. http://dx.doi.org/10.1016/j.jphs.2016.08.001.

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8

Anderson, Carl F. "The Kidney: Physiology and Pathophysiology". Mayo Clinic Proceedings 60, n.º 8 (agosto de 1985): 563. http://dx.doi.org/10.1016/s0025-6196(12)60580-1.

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9

Dunea, George. "The Kidney: Physiology and Pathophysiology". JAMA: The Journal of the American Medical Association 254, n.º 23 (20 de diciembre de 1985): 3373. http://dx.doi.org/10.1001/jama.1985.03360230105035.

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10

Dunea, George. "The Kidney: Physiology and Pathophysiology". JAMA: The Journal of the American Medical Association 267, n.º 23 (17 de junio de 1992): 3216. http://dx.doi.org/10.1001/jama.1992.03480230116042.

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11

Bird, Louise y David Walker. "Pathophysiology of chronic kidney disease". Companion Animal 20, n.º 1 (2 de enero de 2015): 15–19. http://dx.doi.org/10.12968/coan.2015.20.1.15.

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12

Bird, Louise y David Walker. "Pathophysiology of acute kidney injury". Companion Animal 20, n.º 3 (2 de marzo de 2015): 142–47. http://dx.doi.org/10.12968/coan.2015.20.3.142.

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13

Kiss-Tóth, Éva y Tamás Rőszer. "PPARγin Kidney Physiology and Pathophysiology". PPAR Research 2008 (2008): 1–9. http://dx.doi.org/10.1155/2008/183108.

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Involvement of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) in kidney physiology has been explored recently. Synthetic PPARγligands can ameliorate the diabetic kidney disease through different mechanisms, involving inhibition of mesangial cell growth, reduction of mesangial matrix, and cytokine production of glomerular cells as well as promoting endothelial cell survival within the kidney glomeruli. Activation of PPARγhas additional profibrotic consequences, which can contribute to wound healing in diabetic glomerulonephritis. Beside many beneficial effects, PPARγactivation, however, can lead to severe water retention, a common side effect of thiazolidinedione therapy. This unwanted effect is due to the activation of PPARγin the mesonephric distal collecting system, where PPARγpositively regulates sodium and water resorbtion leading to the expansion of interstitial fluid volume. Recent studies indicate that PPARγis also involved in the normal kidney development, renal lipid metabolism, and activation of the renin-angiotensin system. In this paper, we give a synopsis of the current knowledge on PPARγfunctions in kidney phyisology and pathophysiology.

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14

Radi, Zaher A. "Kidney Pathophysiology, Toxicology, and Drug-Induced Injury in Drug Development". International Journal of Toxicology 38, n.º 3 (7 de marzo de 2019): 215–27. http://dx.doi.org/10.1177/1091581819831701.

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Anatomically, the kidneys are paired, bean-shaped (in most mammals), excretory organs that lie in the retroperitoneum. High blood flow to the kidneys, together with high oxygen consumption, makes them more vulnerable to exposure, via the circulation, and subsequent injury related to high concentrations of xenobiotics and chemicals. In preclinical drug development and safety assessment of new investigational drugs, changes in kidney structure and/or function following drug administration in experimental laboratory animals need to be put in context with interspecies differences in kidney functional anatomy, physiology, spontaneous pathologies, and toxicopathological responses to injury. In addition, translation to human relevance to avoid premature drug termination from development is vital. Thus, detection and characterization of kidney toxicity in preclinical species and human relevance will depend on the preclinical safety testing strategy and collective weight-of-evidence approach including new investigational drug mechanism of action (MOA), preclinical and clinical interspecies differences, and MOA relevance to humans. This review describes kidney macroscopic and microscopic functional anatomy, physiology, pathophysiology, toxicology, and drug-induced kidney toxicities in safety risk assessment and drug development.

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15

Paliouras, Christos, Eirini Tsampikaki, Polichronis Alivanis y Georgios Aperis. "Pathophysiology of Nephrolithiasis". Nephrology Research & Reviews 4, n.º 2 (enero de 2012): 58–65. http://dx.doi.org/10.4081/nr.2012.e14.

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The incidence of nephrolithiasis has risen over the last twenty years and continues to rise. Although it is often referred to as a disease, recent advances in the understanding of the pathophysiology suggest that it is a systemic disorder. We conducted a PubMed based literature review on the recent advances in the pathophysiology of kidney stone formation. There is a link between diabetes, metabolic syndrome, obesity, insulin resistance and nephrolithiasis. Along with the aging population and a Western diet, these are the main reasons for the rising incidence and prevalence of nephrolithiasis. Different theories as to the pathophysiological mechanisms of lithogenesis have been proposed, including the free and fixed particle theories, and Randal's plaque hypothesis. Among the different types of kidney stones, those containing calcium are the most common, followed by those containing uric acid, struvite and cystine. Supersaturated urine, acidic urine pH and reductions in kidney stone inhibitors in the urine are the main recognized causes that contribute to the formation of all these stone-types. Nephrolithiasis is considered a systemic pathology that may lead to end-stage renal disease. Although much progress has been made, the underlying pathophysiological mechanisms of kidney stone formation are still not fully understood.

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16

Lewis, Robert. "The pathophysiology underlying chronic kidney disease". Primary Care Cardiovascular Journal (PCCJ) 2, n.º 1 (2009): 11. http://dx.doi.org/10.3132/pccj.2009.028.

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17

Cunningham, Priscilla, Helen Noble, Abdul-Kadhum Al-Modhefer y Ian Walsh. "Kidney stones: pathophysiology, diagnosis and management". British Journal of Nursing 25, n.º 20 (10 de noviembre de 2016): 1112–16. http://dx.doi.org/10.12968/bjon.2016.25.20.1112.

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18

Moe, Orson W. "Kidney stones: pathophysiology and medical management". Lancet 367, n.º 9507 (enero de 2006): 333–44. http://dx.doi.org/10.1016/s0140-6736(06)68071-9.

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19

Sharfuddin, Asif A. y Bruce A. Molitoris. "Pathophysiology of ischemic acute kidney injury". Nature Reviews Nephrology 7, n.º 4 (1 de marzo de 2011): 189–200. http://dx.doi.org/10.1038/nrneph.2011.16.

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20

Epstein, Franklin H. "Book ReviewThe Kidney: Physiology and pathophysiology". New England Journal of Medicine 314, n.º 7 (13 de febrero de 1986): 453–54. http://dx.doi.org/10.1056/nejm198602133140721.

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21

Kanagasundaram, Nigel Suren. "Pathophysiology of ischaemic acute kidney injury". Annals of Clinical Biochemistry 52, n.º 2 (marzo de 2015): 193–205. http://dx.doi.org/10.1177/0004563214556820.

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22

Greenwald, J. E., P. Needleman, M. R. Wilkins y G. F. Schreiner. "Renal synthesis of atriopeptin-like protein in physiology and pathophysiology". American Journal of Physiology-Renal Physiology 260, n.º 4 (1 de abril de 1991): F602—F607. http://dx.doi.org/10.1152/ajprenal.1991.260.4.f602.

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Atriopeptin is synthesized in mammalian atria as a 126-amino acid (14 kDa) prohormone, but it is secreted and circulates as a 28-amino acid (2.5 kDa) peptide. We have demonstrated the synthesis and secretion of an atriopeptin-like peptide in neonatal and adult rat kidney cell cultures. In this study, we evaluated the site of renal synthesis of this protein and its expression in normal rats and rats made nephrotic with puromycin aminonucleoside. The major form of atriopeptin in normal kidneys comigrated with an apparent molecular mass of 2.5 kDa assessed by gel filtration chromatography. However, the major form of this atriopeptin-like protein in nephrotic kidneys was determined to have an apparent molecular mass similar to the heart prohormone. No atriopeptin prohormone was detected in the plasma of nephrotic rats. Localization of this renal atriopeptin-like protein was accomplished by immunocytochemistry of rat kidney frozen sections. Using an antibody generated against either the COOH-terminal or NH3-terminal region of the cardiac atriopeptin prohormone, we detected specific immunostaining in the distal cortical nephron of the nephrotic kidney. This is the first report of the anatomic localization of a renal atriopeptin-like protein and its upregulation in nephrosis.

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23

Masood, Humaira, Ruochen Che y Aihua Zhang. "Inflammasomes in the Pathophysiology of Kidney Diseases". Kidney Diseases 1, n.º 3 (2015): 187–93. http://dx.doi.org/10.1159/000438843.

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Background: The inflammasome is a complex of proteins in the cytoplasm that consists of three main components: a sensor protein (receptor), an adapter protein and caspase-1. Inflammasomes are the critical components of innate immunity and have been gradually recognized as a critical mediator in various autoimmune diseases; also, their role in chronic kidney disease and acute kidney injury has been gradually accepted. Summary: Inflammasomes triggered by infectious or sterile injuries transfer proinflammatory mediators into mature ones through innate danger-signaling platforms. Information on inflammasomes in kidney disease will help to uncover the underlying mechanisms of nephropathy and provide novel therapeutic targets in the future. Key Messages: The inflammasomes can be activated by a series of exogenous and endogenous stimuli, including pathogen-and danger-associated molecular patterns released from or caused by damaged cells. The NACHT, LRR and PYD domain-containing protein 3 (NLRP3) in the kidney exerts its effect not only by the ‘canonical' pathway of IL-1β and IL-18 secretion but also by ‘noncanonical' pathways, such as tumor growth factor-β signaling, epithelial-mesenchymal transition and fibrosis. In both clinical and experimental data, the NLRP3 inflammasome was reported to be involved in the pathogenesis of chronic kidney disease and acute kidney injury. However, the underlying mechanisms are not fully understood. Therapies targeting the activation of the NLRP3 inflammasome or blocking its downstream effectors appear attractive for the pursuit of neuropathy treatments.

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24

Ozkok, Abdullah y Charles L. Edelstein. "Pathophysiology of Cisplatin-Induced Acute Kidney Injury". BioMed Research International 2014 (2014): 1–17. http://dx.doi.org/10.1155/2014/967826.

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Cisplatin and other platinum derivatives are the most widely used chemotherapeutic agents to treat solid tumors including ovarian, head and neck, and testicular germ cell tumors. A known complication of cisplatin administration is acute kidney injury (AKI). The nephrotoxic effect of cisplatin is cumulative and dose-dependent and often necessitates dose reduction or withdrawal. Recurrent episodes of AKI may result in chronic kidney disease. The pathophysiology of cisplatin-induced AKI involves proximal tubular injury, oxidative stress, inflammation, and vascular injury in the kidney. There is predominantly acute tubular necrosis and also apoptosis in the proximal tubules. There is activation of multiple proinflammatory cytokines and infiltration of inflammatory cells in the kidney. Inhibition of the proinflammatory cytokines TNF-αor IL-33 or depletion of CD4+ T cells or mast cells protects against cisplatin-induced AKI. Cisplatin also causes endothelial cell injury. An understanding of the pathogenesis of cisplatin-induced AKI is important for the development of adjunctive therapies to prevent AKI, to lessen the need for dose decrease or drug withdrawal, and to lessen patient morbidity and mortality.

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25

Agarwal, Rajiv. "Diabetic kidney disease: pathophysiology, implications and management". Trends in Endocrinology & Metabolism 17, n.º 2 (marzo de 2006): 38–39. http://dx.doi.org/10.1016/j.tem.2005.12.001.

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26

Sałata, Daria y Barbara Dołęgowska. "Bioactive lipids in kidney physiology and pathophysiology". Postępy Higieny i Medycyny Doświadczalnej 68 (24 de enero de 2014): 73–83. http://dx.doi.org/10.5604/17322693.1086412.

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27

Srinivas, Rashmi y S. Vishwanath. "Pathophysiology of Hypertension in Chronic Kidney Disease". Hypertension Journal 4, n.º 3 (2018): 166–69. http://dx.doi.org/10.15713/ins.johtn.0126.

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28

Schnaper, H. William. "The Tubulointerstitial Pathophysiology of Progressive Kidney Disease". Advances in Chronic Kidney Disease 24, n.º 2 (marzo de 2017): 107–16. http://dx.doi.org/10.1053/j.ackd.2016.11.011.

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29

Kohan, Donald E. "Endothelins in the Kidney: Physiology and Pathophysiology". American Journal of Kidney Diseases 22, n.º 4 (octubre de 1993): 493–510. http://dx.doi.org/10.1016/s0272-6386(12)80920-6.

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30

Toth-Manikowski, Stephanie y Mohamed G. Atta. "Diabetic Kidney Disease: Pathophysiology and Therapeutic Targets". Journal of Diabetes Research 2015 (2015): 1–16. http://dx.doi.org/10.1155/2015/697010.

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Diabetes is a worldwide epidemic that has led to a rise in diabetic kidney disease (DKD). Over the past two decades, there has been significant clarification of the various pathways implicated in the pathogenesis of DKD. Nonetheless, very little has changed in the way clinicians manage patients with this disorder. Indeed, treatment is primarily centered on controlling hyperglycemia and hypertension and inhibiting the renin-angiotensin system. The purpose of this review is to describe the current understanding of how the hemodynamic, metabolic, inflammatory, and alternative pathways are all entangled in pathogenesis of DKD and detail the various therapeutic targets that may one day play a role in quelling this epidemic.

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31

Akilesh, Shreeram, Noemie Juaire, Jeremy S. Duffield y Kelly D. Smith. "Chronic Ifosfamide Toxicity: Kidney Pathology and Pathophysiology". American Journal of Kidney Diseases 63, n.º 5 (mayo de 2014): 843–50. http://dx.doi.org/10.1053/j.ajkd.2013.11.028.

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32

Bonventre, Joseph V. y Li Yang. "Cellular pathophysiology of ischemic acute kidney injury". Journal of Clinical Investigation 121, n.º 11 (1 de noviembre de 2011): 4210–21. http://dx.doi.org/10.1172/jci45161.

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33

Rosa, Ciro Dalla. "Book Review: The Kidney: Physiology and Pathophysiology". Urologia Journal 59, n.º 1 (febrero de 1992): 111–12. http://dx.doi.org/10.1177/039156039205900136.

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34

Geenen, Remy W. F., Hylke Jan Kingma y Aart J. van der Molen. "Pathophysiology of Contrast-Induced Acute Kidney Injury". Interventional Cardiology Clinics 3, n.º 3 (julio de 2014): 363–67. http://dx.doi.org/10.1016/j.iccl.2014.03.007.

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35

Bansal, Shweta y Rahul N. Patel. "Pathophysiology of Contrast-Induced Acute Kidney Injury". Interventional Cardiology Clinics 9, n.º 3 (julio de 2020): 293–98. http://dx.doi.org/10.1016/j.iccl.2020.03.001.

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36

Bhatt, Kirti, Mitsuo Kato y Rama Natarajan. "Mini-review: emerging roles of microRNAs in the pathophysiology of renal diseases". American Journal of Physiology-Renal Physiology 310, n.º 2 (15 de enero de 2016): F109—F118. http://dx.doi.org/10.1152/ajprenal.00387.2015.

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MicroRNAs (miRNA) are endogenously produced short noncoding regulatory RNAs that can repress gene expression by posttranscriptional mechanisms. They can therefore influence both normal and pathological conditions in diverse biological systems. Several miRNAs have been detected in kidneys, where they have been found to be crucial for renal development and normal physiological functions as well as significant contributors to the pathogenesis of renal disorders such as diabetic nephropathy, acute kidney injury, lupus nephritis, polycystic kidney disease, and others, due to their effects on key genes involved in these disease processes. miRNAs have also emerged as novel biomarkers in these renal disorders. Due to increasing evidence of their actions in various kidney segments, in this mini-review we discuss the functional significance of altered miRNA expression during the development of renal pathologies and highlight emerging miRNA-based therapeutics and diagnostic strategies for early detection and treatment of kidney diseases.

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37

Martin, Rhonda K. "Acute Kidney Injury". AACN Advanced Critical Care 21, n.º 4 (1 de octubre de 2010): 350–56. http://dx.doi.org/10.4037/nci.0b013e3181f9574b.

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Acute kidney injury (AKI) is a common disease in the acutely ill patient population, as a singular diagnosis or a complication of sepsis, causing significant mortality and morbidity. Progress in diagnosis, treatment, and research in AKI has been limited by the lack of a universally accepted clinical definition. The clinical definition of AKI onset and progression, early diagnostic indicators, and understanding the unique pathophysiology of AKI are requisite to early treatment and management and ultimately positive patient outcomes. This article reviews the advances in defining and staging AKI on the basis of international consensus statements. An update on the most recent concepts affecting renal pathophysiology in AKI is also presented. Current clinical tools used in diagnosing and monitoring AKI, including the development of renal biomarkers, are discussed.

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38

Neki, NS. "Cardiorenal Syndrome - A Review Article". Journal of Medicine 16, n.º 1 (25 de febrero de 2015): 39–45. http://dx.doi.org/10.3329/jom.v16i1.22400.

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Cardiorenal syndromes (CRS) describe the dynamic inter-relationship between heart and kidney malfunction. Recent studies have clearly defined its various types and pathophysiology. Improved survival, cardiovascular risk factors (diabetes, hypertension, dyslipidemia), diagnostic and therapeutic intervention are some contributors in its causation. Types 1 and 2 CRS involve acute and chronic cardiovascular disease (CVD) scenarios leading to acute kidney injury or accelerated chronic kidney disease. Types 3 and 4 CRS describe acute and chronic kidney disease leading primarily to heart failure, although it is possible that acute coronary syndromes, stroke, and arrhythmias could be CVD outcomes in these forms of CRS. Finally, CRS type 5 describes a simultaneous insult to both heart and kidneys, such as sepsis, where both organs are injured simultaneously. This article focuses on different types, pathophysiology, novel biomarkers, preventive and treatment aspects of cardiorenal syndromes.DOI: http://dx.doi.org/10.3329/jom.v16i1.22400 J MEDICINE 2015; 16 : 39-45

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39

Kinaan, Mustafa, Hanford Yau, Suzanne Quinn Martinez y Pran Kar. "Concepts in Diabetic Nephropathy: From Pathophysiology to Treatment". Journal of Renal and Hepatic Disorders 1, n.º 2 (29 de junio de 2017): 10–24. http://dx.doi.org/10.15586/jrenhep.2017.17.

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Since the 1930s when Kimmelstiel and Wilson first described the classic nodular glomerulosclerosis lesions in diabetic kidneys, nephropathy has been recognized as a major and common complication of diabetes. Nearly 40% of diabetics around the world have microalbuminuria, a marker of progression to chronic kidney disease (CKD). Diabetic kidney disease (DKD) is also considered a leading cause of CKD worldwide. Given the significant morbidity, mortality, and health-care burden, several clinical and scientific societies continue to seek a better understanding of this disease. Screening for microalbuminuria and controlling hyperglycemia remain the pillars for the prevention of diabetic nephropathy. However, evidence from multiple studies suggests that controlling DKD is more challenging. Some studies suggest that there is variability in the incidence of renal complications among patients despite comparable hyperglycemic control. Therefore, there has been great interest in studying the inherent, renal protective role of the different antihyperglycemic agents. This review will shed light on the pathophysiology, screening, and diagnosis of DKD. It will also discuss the treatment and prevention of diabetic nephropathy, with a specific focus on comparing the mechanisms, safety profiles, and efficacy of the different antihyperglycemic medications.

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40

Kadir, Akmarawita. "Hubungan Patofisiologi Hipertensi dan Hipertensi Renal". Jurnal Ilmiah Kedokteran Wijaya Kusuma 5, n.º 1 (13 de febrero de 2018): 15. http://dx.doi.org/10.30742/jikw.v5i1.2.

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Introduction : Hypertension is a disease with an incidence rate is still high around the world, most of the causes of hypertension is unknown (essential hypertension / primary hypertension), a small portion of hypertension caused by diseases acquired (secondary hypertension). The unknown cause of Hypertension causing complications of diseases that worsen it, eg kidney disease (renal disease), and can be a disease that actually cause hypertension becomes more severe (secondary hypertension). Pathophysiology of essential hypertension has been a lot of discussed, but the pathophysiology of renal disease which causes hypertension still needs to be explored, particularly on the relationship between primary hypertension and secondary hypertension (hypertension, kidney or renal hypertention). Kidney disease is a disease that cause hypertension via the mechanism of resistance increases blood circulation to the kidneys and a decrease in the glomerular capillary function which resulted in the release of an important substance-substance such as renin, angiotensinogen, angiotensin I, angiotensin II, angiotensin converting enzyme (ACE) inhibitors, aldosterone, bradykinin, nitric oxide (NO), which in turn causes increase blood pressure (hypertension). Hypertension proved to be a feedback mechanism to suppress the high renin, renin suppression doesn’t mean anything if kidney disease not treated properly, and even cause permanently hypertension or even getting worse. The purpose of this article was to determine the pathophysiology of hypertension, renal hypertension in particular, and how the relationship between hypertension and renal hypertension (secondary).

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41

Horino, Taro y Yoshio Terada. "II. Epidemiology and Pathophysiology of Acute Kidney Injury". Nihon Naika Gakkai Zasshi 103, n.º 5 (2014): 1055–60. http://dx.doi.org/10.2169/naika.103.1055.

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42

Tamura, Kouichi. "2. Pathophysiology of Atherosclerosis in Chronic Kidney Disease". Nihon Naika Gakkai Zasshi 105, n.º 5 (2016): 802–10. http://dx.doi.org/10.2169/naika.105.802.

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43

Vlachopanos, Georgios, Dimitrios Schizas, Natasha Hasemaki y Argyrios Georgalis. "Pathophysiology of Contrast-Induced Acute Kidney Injury (CIAKI)". Current Pharmaceutical Design 25, n.º 44 (9 de enero de 2020): 4642–47. http://dx.doi.org/10.2174/1381612825666191210152944.

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: Contrast-induced acute kidney injury (CIAKI) is a severe complication associated with the use of iodinated contrast media (CM); a sudden but potentially reversible fall in glomerular filtration rate (GFR) typically occurring 48-72 hours after CM administration. Principal risk factors related with the presentation of CIAKI are preexisting chronic kidney disease and diabetes mellitus. Studies on CIAKI present considerable complexity because of differences in CM type and dose, controversies in definition and baseline comorbidities. Despite that, it should be noted that CIAKI poses a serious health problem because it is a very common cause of hospitalacquired AKI, linked to increased morbidity and mortality and utilizing growing healthcare resources. The pathogenesis of CIAKI is heterogeneous and, thus, is incompletely understood. Three basic mechanisms appear to simultaneously occur for CIAKI development: Renal vasoconstriction and medullary hypoxia, tubular cell toxicity and reactive oxygen species formation. The relative contribution of each one of these mechanisms is unknown but they ultimately lead to epithelial and endothelial cell apoptosis and GFR reduction. Further research is needed in order to better clarify CIAKI pathophysiology and accordingly introduce effective preventive and therapeutic strategies.

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44

Coe, Fredric L., Andrew Evan y Elaine Worcester. "Pathophysiology-Based Treatment of Idiopathic Calcium Kidney Stones". Clinical Journal of the American Society of Nephrology 6, n.º 8 (agosto de 2011): 2083–92. http://dx.doi.org/10.2215/cjn.11321210.

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45

Dawson, Charlotte H. y Charles RV Tomson. "Kidney stone disease: pathophysiology, investigation and medical treatment". Clinical Medicine 12, n.º 5 (octubre de 2012): 467–71. http://dx.doi.org/10.7861/clinmedicine.12-5-467.

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Campese, Vito M. "Pathophysiology of Resistant Hypertension in Chronic Kidney Disease". Seminars in Nephrology 34, n.º 5 (septiembre de 2014): 571–76. http://dx.doi.org/10.1016/j.semnephrol.2014.08.011.

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Rapoport, J. "Autosomal dominant polycystic kidney disease: pathophysiology and treatment". QJM 100, n.º 1 (17 de diciembre de 2006): 1–9. http://dx.doi.org/10.1093/qjmed/hcl129.

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Metzinger-Le Meuth, Valérie, Ophélie Fourdinier, Nathalie Charnaux, Ziad A. Massy y Laurent Metzinger. "The expanding roles of microRNAs in kidney pathophysiology". Nephrology Dialysis Transplantation 34, n.º 1 (25 de mayo de 2018): 7–15. http://dx.doi.org/10.1093/ndt/gfy140.

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Coe, Fredric L. y Joan H. Parks. "Pathophysiology of Kidney Stones and Strategies for Treatment". Hospital Practice 23, n.º 3 (15 de marzo de 1988): 185–207. http://dx.doi.org/10.1080/21548331.1988.11703444.

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Kanasaki, Keizo, Munehiro Kitada y Daisuke Koya. "Pathophysiology of the aging kidney and therapeutic interventions". Hypertension Research 35, n.º 12 (18 de octubre de 2012): 1121–28. http://dx.doi.org/10.1038/hr.2012.159.

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